ArticleDiabetes2017
Overexpression of Kinase-Dead mTOR Impairs Glucose Homeostasis by Regulating Insulin Secretion and Not β-Cell Mass.
Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- A homozygous TARS2 variant is a novel cause of syndromic neonatal diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2025Article
- mTOR Variants Activation Discovers PI3K-like Cryptic Pocket, Expanding Allosteric, Mutant-Selective Inhibitor Designs.Journal of chemical information and modeling · 2025Article
- Sweet Spot Regulation of Maternal Metabolic Health and Nutrition on β-Cell Mass in the Offspring.Advances in anatomy, embryology, and cell biology · 2024Review
- Epigenome wide association study in peripheral blood of pregnant women identifies potential metabolic pathways related to gestational diabetes.Epigenetics · 2023Article
- Sex Differences in Pancreatic β-Cell Physiology and Glucose Homeostasis in C57BL/6J Mice.Journal of the Endocrine Society · 2023Article
- Time-dependent effects of endogenous hyperglucagonemia on glucose homeostasis and hepatic glucagon action.JCI insight · 2023Article
- Architecture of androgen receptor pathways amplifying glucagon-like peptide-1 insulinotropic action in male pancreatic β cells.Cell reports · 2023Article
- Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022Article
- Novel roles of mTORC2 in regulation of insulin secretion by actin filament remodeling.American journal of physiology. Endocrinology and metabolism · 2022Article
- Maturation of beta cells: lessons from in vivo and in vitro models.Diabetologia · 2022Review
- Review
- Molecular pathways dysregulated by PbToxicology research · 2022Article
- Regulation of Pdx1 by oxidative stress and Nrf2 in pancreatic beta-cells.Frontiers in endocrinology · 2022Review
- Endocrine Regulation of Lifespan in Insect Diapause.Frontiers in physiology · 2022Review
- Pancreatic Differentiation of Stem Cells Reveals Pathogenesis of a Syndrome of Ketosis-Prone Diabetes.Diabetes · 2021Article
- The RNA-binding protein LARP1 is dispensable for pancreatic β-cell function and mass.Scientific reports · 2021Article
- TBK1 regulates regeneration of pancreatic β-cells.Scientific reports · 2020Article
- Metabolic Role of PTEN in Insulin Signaling and Resistance.Cold Spring Harbor perspectives in medicine · 2020Review
- A Nutrient-Sensing Transition at Birth Triggers Glucose-Responsive Insulin Secretion.Cell metabolism · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Regulation of glucose homeostasis by insulin depends on β-cell growth and function. Nutrients and growth factor stimuli converge on the conserved protein kinase mechanistic target of rapamycin (mTOR), existing in two complexes, mTORC1 and mTORC2. To understand the functional relevance of mTOR enzymatic activity in β-cell development and glucose homeostasis, we generated mice overexpressing either one or two copies of a kinase-dead mTOR mutant (KD-mTOR) transgene exclusively in β-cells. We examined glucose homeostasis and β-cell function of these mice fed a control chow or high-fat diet. Mice with two copies of the transgene [RIPCre;KD-mTOR (Homozygous)] develop glucose intolerance due to a defect in β-cell function without alterations in β-cell mass with control chow. Islets from RIPCre;KD-mTOR (Homozygous) mice showed reduced mTORC1 and mTORC2 signaling along with transcripts and protein levels of Pdx-1. Islets with reduced mTORC2 signaling in their β-cells (RIPCre;Rictor
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.